Abstract | AIM: METHODS: Sixty-two patients with advanced colorectal cancer were genotyped, using allele-specific primers and SYBR green in real-time polymerase chain reaction. All patients had received adjuvant oxalipla- tin-based chemotherapy. The severity of OXLIPN was defined by means of the clinical total neuropathy score. Following the discontinuation of treatment, 36/62 patients (58.1%) developed OXLIPN. Grade I neurotoxicity was revealed in 14 (38.9%) patients and grade II neurotoxicity in 22 (61.1%) patients. RESULTS: From patients without OXLIPN (n = 26), 80.8% (n = 21) were homozygous for G, 19.2% (n = 5) were heterozygous (AG) and none was homozygous for A. The corresponding percentages for patients developing any grade of OXLIPN (n = 36) were similar. Likewise, among patients experiencing OXLIPN, insignificant differences in R19K genotypes were revealed between those with grade I versus grade II neurotoxicity. CONCLUSION: Our study failed to provide evidence to support a causal relationship between the SCN2A R19K polymorphism and OXLIPN.
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Authors | Andreas A Argyriou, Anna G Antonacopoulou, Chrisoula D Scopa, Anastasia Kottorou, Athina Kominea, Stavros Peroukides, Haralabos P Kalofonos |
Journal | Oncology
(Oncology)
Vol. 77
Issue 3-4
Pg. 254-6
( 2009)
ISSN: 1423-0232 [Electronic] Switzerland |
PMID | 19738391
(Publication Type: Journal Article)
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Copyright | Copyright 2009 S. Karger AG, Basel. |
Chemical References |
- Antineoplastic Agents
- NAV1.2 Voltage-Gated Sodium Channel
- Nerve Tissue Proteins
- Organoplatinum Compounds
- SCN2A protein, human
- Sodium Channels
- Oxaliplatin
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Topics |
- Aged
- Antineoplastic Agents
(adverse effects)
- Female
- Humans
- Male
- Middle Aged
- NAV1.2 Voltage-Gated Sodium Channel
- Nerve Tissue Proteins
(genetics)
- Organoplatinum Compounds
(adverse effects)
- Oxaliplatin
- Peripheral Nervous System Diseases
(chemically induced)
- Polymorphism, Genetic
- Sodium Channels
(genetics)
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